Second‑generation, irreversible pan‑HER tyrosine kinase inhibitor that covalently inhibits EGFR (HER1), HER2, and HER4, blocking downstream signaling (e.g., MAPK/PI3K‑AKT) to suppress proliferation and induce apoptosis in tumors driven by these receptors.
Dacomitinib irreversibly inhibits HER2 kinase activity, blocking MAPK/PI3K–AKT signaling and inducing growth arrest and apoptosis in HER2-dependent cells.
Polyclonal antibody preparation that depletes T lymphocytes for induction immunosuppression.
Polyclonal anti–T-lymphocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity and Fc-mediated ADCC, with additional T-cell apoptosis and functional inhibition, producing potent immunosuppression.
ATG binds CD5 (among other T‑cell antigens) and triggers complement-dependent cytotoxicity and Fc-mediated ADCC, also inducing apoptosis, thereby depleting CD5+ cells.
Second‑generation, irreversible pan‑HER tyrosine kinase inhibitor that covalently inhibits EGFR (HER1), HER2, and HER4, blocking downstream signaling (e.g., MAPK/PI3K‑AKT) to suppress proliferation and induce apoptosis in tumors driven by these receptors.
Dacomitinib irreversibly inhibits HER4 tyrosine kinase, blocking MAPK/PI3K–AKT survival signaling and inducing growth arrest and apoptosis in HER4-dependent cells.
Third-generation EGFR inhibitor active against T790M with CNS penetration.
Third‑generation, orally available, irreversible and mutant‑selective EGFR tyrosine kinase inhibitor that covalently binds EGFR at C797, potently inhibiting mutant forms including T790M, L858R, and exon 19 deletions, thereby blocking EGFR signaling, suppressing tumor growth, and inducing cancer cell death; demonstrates CNS penetration and relatively spares wild‑type EGFR.
Covalent inhibition of mutant EGFR (L858R) at C797 blocks EGFR signaling (e.g., PI3K/AKT/ERK), leading to growth arrest and apoptosis of EGFR-dependent tumor cells.